Recurrent stroke risk in intracranial atherosclerotic disease (original) (raw)
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BMC Neurology, 2019
Background: This study examined how intracranial large artery stenosis (ILAS), symptomatic and asymptomatic ILAS, and risk factors affect unfavorable outcome events after medical treatment in routine clinical practice. Methods: This was a 24-month prospective observational study of consecutively recruited stroke patients. All participants underwent magnetic resonance angiography, and their clinical characteristics were assessed. Outcome events were vascular outcome, recurrent stroke, and death. Cox regression analyses were performed to identify potential factors associated with an unfavorable outcome, which included demographic and clinical characteristics, the risk factors, and stenosis status. Results: The analysis included 686 patients; among them, 371 were assessed as ILAS negative, 231 as symptomatic ILAS, and 84 as asymptomatic ILAS. Body mass index (p < .05), hypertension (p = .01), and old infarction (p = .047) were factors relating to vascular outcomes. Hypertension was the only factor for recurrent stroke (p = .035). Poor glomerular filtration rate (< 30 mL/min/1.73 m 2) (p = .011) and baseline National Institutes of Health Stroke Scale scores (p < .001) were significant predictors of death. Conclusions: This study extended previous results from clinical trials to a community-based cohort study by concurrently looking at the presence/absence of stenosis and a symptomatic/asymptomatic stenotic artery. Substantiated risk factors rather than the stenosis status were predominant determinants of adverse outcome. Although the degree of stenosis is often an indicator for treatment, we suggest risk factors, such as hypertension and renal dysfunction, should be monitored and intensively treated.
Circulation, 2007
MB, ChB; for the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) Trial Investigators Background-Many clinicians allow blood pressure to run high in patients with intracranial stenosis to protect against hypoperfusion. We sought to determine whether higher blood pressure decreases the risk of stroke in these patients. Methods and Results-Data on 567 patients in the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial were analyzed. Time to ischemic stroke and stroke in the same territory of the stenotic vessel was compared in patients grouped by mean systolic blood pressure (SBP) and mean diastolic blood pressure (DBP) during the study. Additional analyses were based on severity and location of stenosis. Ischemic stroke risk increased with increasing mean SBP and DBP on univariate analysis (PϽ0.0001, PϽ0.0001) and after adjustment for risk factors (Pϭ0.0008, PϽ0.0001). Elevated mean SBP and DBP also resulted in increased risk of stroke in the territory in univariate (Pϭ0.0065, PϽ0.0001) and adjusted (Pϭ0.0002, Pϭ0.0005) analyses. The increased risk of stroke with increasing SBP was driven largely by patients in the highest SBP group. Patients with moderate (Ͻ70%) stenosis had increased risk of stroke (PϽ0.0001, Pϭ0.003) and stroke in the territory (Pϭ0.0002, Pϭ0.010) with increased SBP and DBP. Patients with severe (Ն70%) stenosis had increased risk of stroke and stroke in the territory with elevated DBP (Pϭ0.004, Pϭ0.004). Conclusions-In patients with intracranial stenosis, higher blood pressure is associated with increased (not decreased) risk of ischemic stroke and stroke in the territory of the stenotic vessel. These findings argue strongly against the common clinical practice of maintaining high blood pressure in patients with intracranial stenosis. (Circulation. 2007;115:2969-2975.)
Hemostatic Markers in Patients at Risk of Cerebral Ischemia
Stroke, 2000
Background-Increased levels of markers of hemostasis may assist in the determination of the extent of carotid occlusive disease and the identification of neurologically intact individuals at increased risk of ischemic events. Methods-We conducted a prospective study of 304 subjects, including 82 with a recent (Յ7 days) transient ischemic attack (TIA), 157 asymptomatic individuals with a cervical bruit, and 65 control subjects. Baseline evaluation included a neurological assessment, ECG, cervical ultrasonography, and cerebral CT and/or MRI. Levels of markers of coagulation and fibrinolytic activity were also determined. Results were analyzed in relation to the degree of carotid disease and the subsequent occurrence of cerebral and cardiac ischemic events. Results-Over a mean follow-up period of 2.8 years (SD, 1.3 years), 114 ischemic events occurred. Survival analyses showed that prothrombin fragment 1.2 (F 1.2 ) was a predictor of time to cerebral and cardiac ischemic events in the combined TIA and asymptomatic bruit group (relative risk [RR], 1.46; 95% CI, 1.18 to 1.81) as well as in the asymptomatic bruit group separately (RR, 1.70; 95% CI, 1.14 to 2.53). In the TIA group, both F 1.2 (RR, 2.36; 95% CI, 1.19 to 4.68) and severe (Ն80%) carotid stenosis (RR, 3.53; 95% CI, 1.19 to 10.51) were predictive of time to ischemic stroke, myocardial infarction, or vascular death. Conclusions-In patients with TIAs and in asymptomatic individuals with cervical bruits, F 1.2 levels were found to be independent predictors of subsequent cerebral and cardiac ischemic events. Our results are consistent with an active role of the coagulation system through upregulation of thrombin in carotid disease progression and in the pathogenesis of ischemic events in patients at risk. (Stroke. 2000;31:1856-1862.)
Hemodynamics and stroke risk in intracranial atherosclerotic disease
Annals of Neurology, 2019
To investigate whether hemodynamic features of symptomatic intracranial atherosclerotic stenosis (sICAS) might correlate with the risk of stroke relapse, using a computational fluid dynamics (CFD) model. Methods: In a cohort study, we recruited patients with acute ischemic stroke attributed to 50-99% ICAS confirmed in CT angiography (CTA). With CTA-based CFD models, translesional pressure ratio (PR
Consensus Conference on Intracranial Atherosclerotic Disease: Rationale, Methodology, and Results
Journal of Neuroimaging, 2009
The consensus conference on intracranial atherosclerotic disease (ICAD) identifies principles of management, and research priorities in various aspects upon which leading experts can agree (using "Delphi" method). ICAD is more prevalent in Asian, Hispanic, and African-American populations. Patients who have had a stroke or transient ischemic attack (TIA) attributed to stenosis (50-99%) of a major intracranial artery face a 12-14% risk of subsequent stroke during the 2-year period after the initial ischemic event, despite treatment with antithrombotic medications. The annual risk of subsequent stroke may exceed 20% in high-risk groups. The medical treatment of patients with symptomatic ICAD is directed toward: 1. Prevention of intraluminal thrombo-embolism, 2. plaque stabilization and regression, and 3. management of atherogenic risk factors. In patients with ICAD, short-term and long-term anticoagulation (compared with aspirin) have not shown to be beneficial. The current guidelines recommend that aspirin monotherapy, the combination of aspirin and extended release dipyridamole, and clopidogrel monotherapy (rather than oral anticoagulants) are all acceptable options in patients with non-cardioembolic ischemic stroke and TIA. Overall, the subgroup analysis from randomized trials provides evidence about benefit of aggressive atherogenic risk factor management among patients with ICAD. Intracranial angioplasty with or without stent placement has evolved as a therapeutic option for patients with symptomatic ICAD, particularly those with highgrade stenosis with recurrent ischemic symptoms and/or medication failure. A matched comparison between medical-treated patients in the Warfarin Aspirin Symptomatic Intracranial Disease (WASID) study and stent-treated patients in the National Institutes of Health intracranial stent registry concluded that stent placement may offer benefit in patients with 70-99% stenosis. The 5-year, multicenter, prospective, randomized Stenting and Aggressive Medical Management for Preventing Recurrent stroke in Intracranial Stenosis study supported by the National Institutes of Health is currently comparing stent placement with intense medical management with intense medical management alone in patients with high-grade symptomatic intracranial stenosis. The proceedings of the consensus conference provide a template for standardizing management of patients with ICAD and determining research priorities.
Journal of Stroke and Cerebrovascular Diseases, 2020
Background: Non-stenotic intracranial and systemic atherosclerosis are associated with ischemic stroke. We report frequency and response to anticoagulant vs. antiplatelet prophylaxis of patients with embolic stroke of undetermined source (ESUS) who have non-stenotic intracranial atherosclerosis and/or systemic atherosclerosis. Methods: Exploratory analysis of the international NAVIGATE ESUS randomized trial comparing rivaroxaban 15mg daily with aspirin 100mg daily in 7213 patients with recent ESUS. Among participants with results of intracranial arterial imaging with either computed tomographic angiography (CTA) or magnetic resonance angiography (MRA), the frequency and predictors of non-stenotic intracranial and systemic atherosclerosis and responses to antithrombotic therapy were assessed. Results: Among 4723 participants with available intracranial CTA or MRA results (65% of the trial cohort), the prevalence of intracranial atherosclerosis was 16% (n=739). Patient features independently associated with intracranial atherosclerosis included East Asian region (odds ratio 2.7, 95%CI 2.2,3.3) and cervical carotid plaque (odds ratio 2.3, 95%CI 1.9,2.7), among others. The rate of recurrent ischemic stroke averaged 4.8%/year among those with intracranial atherosclerosis vs. 5.0.%/year for those without (HR 0.95, 95%CI 0.65, 1.4). Among those with intracranial atherosclerosis, the recurrent ischemic stroke rate was higher if assigned to rivaroxaban (5.8%/year) vs. aspirin (3.7%/year), but the difference was not From the
Cerebrovascular Diseases, 2014
WASID) trial. We defined the likely mechanism of stroke (artery-to-artery embolism, perforator occlusion, hypoperfusion or mixed) according to the site of ICAS and based on the infarct patterns on neuroimaging. Collaterals were assessed using American Society of Interventional and Therapeutic Neuroradiology/Society of Interventional Radiology (ASITN/ SIR) grades, and stenosis severity using the WASID trial's measurement technique. We evaluated the association of infarct patterns with angiographic features using χ 2 tests. Results: The likely mechanisms of stroke based on the infarct patterns at baseline in the 136 patients included in the study were artery-to-artery embolism (n = 69; 50.7%), perforator occlusion (n = 34; 25%), hypoperfusion (n = 12; 8.8%) and mixed (n = 21; 15.5%). Perforator-occlusive infarcts were Abstract Background: There are limited data on the specific mechanisms of stroke in patients with intracranial atherosclerotic stenosis (ICAS). We undertook this study to describe infarct patterns and likely mechanisms of stroke in a large cohort of patients with ICAS, and to evaluate the relationship of these infarct patterns to angiographic features (collaterals, stenosis location and stenosis severity). Methods: We evaluated infarct patterns in the territory of a stenotic intracranial artery on neuroimaging performed at baseline and during follow-up if a recurrent stroke occurred in patients enrolled in the Warfarin-Aspirin Symptomatic Intracranial Disease
Stroke, 2005
Background and Purpose-Optimization of coronary risk evaluation in stroke patients has been encouraged. The relationship between symptomatic intracranial atherosclerosis and occult coronary artery disease (CAD) has not been evaluated sufficiently. We aimed to investigate the prevalence of silent myocardial ischemia in patients with symptomatic intracranial atherosclerosis and to identify factors associated with its presence. Methods-From 186 first-ever transient ischemic attack or ischemic stroke patients with intracranial stenoses, 65 fulfilled selection criteria, including angiographic confirmation of a symptomatic atherosclerotic stenosis and absence of known CAD. All patients underwent a maximal-stress myocardial perfusion single-photon emission computed tomography (SPECT). Lipoprotein(a) [Lp(a)], C-reactive protein, and homocysteine (Hcy) levels were determined before SPECT.
Journal of Atherosclerosis and Thrombosis, 2016
New ischemic lesions in the brain can be detected in approximately 50% of patients undergoing carotid artery stenting (CAS). We wished to discover the laboratory-based predictors of new infarctions in the brain after CAS. Methods: All consecutive patients with internal carotid artery stenosis of ≥ 70% with indication for CAS were enrolled in a prospective study for 16 months. All patients used dual antiplatelet therapy for ≥ 7 days before CAS. Neurologic examination and magnetic resonance imaging (MRI) of the brain were undertaken before and at 24 h after CAS. Samples of venous blood were collected at 24 h before CAS for the evaluation of hematology, reticulocytes, coagulation markers (PT, APTT, Fbg, Clauss), vWF antigen, PAI-1 activity, PAI-1 polymorphism 4G/5G, and the multiplate (aspirin and clopidogrel) resistance test. Blood samples for the assessment of anti-Xa activity were collected during CAS. Differences in the values of laboratory markers between patients with and without new ischemic lesions of the brain on control MRI were evaluated. Results: The cohort comprised 81 patients (53 males; mean age, 67.3 7.2 years). New ischemic infarctions in the brain on control MRI were found in 46 (56.8%) patients. Three of seven patients with resistance to aspirin or clopidogrel had a new ischemic infarction in the brain. No significant differences for particular markers were found between patients with and without an ischemic lesion in the brain. Conclusion: A high risk of a new ischemic infarction in the brain was detected in patients undergoing CAS, but a laboratory-based predictor of such an infarction could not be identified.